Bacterial plasmids have been used to study repair and mutagenesis of benzopyrene diol epoxide (BPDE)-damaged DNA in E. coli. In "nontargeted" experiments, the plasmids were randomly modified by BPDE and introduced into E. coli strains which differed in their capacity for repair and mutagenesis. By measuring both the survival of bacteria containing plasmids and the mutagenesis of a plasmid gene, it was possible to identify host cell functions for error-free repair and for mutagenesis. It was found that repair functions can be distinguished temporally from mutagenic activities after induction of the inducible repair response (SOS). In "targeted" experiments, a specific fragment of the plasmid from a nonessential marker gene was modified with BPDE and ligated back into the plasmid. The survival curves of these constructs were virtually identical to those of the randomly modified plasmids, suggesting that the principal determinant for survival of BPDE-damaged DNA is the simple presence of the carcinogen, rather than secondary mutational events in essential functions. Furthermore, plasmid survival was a function of the adduct/plasmid, not the adduct/nucleotide, ratio. Mutants were found in the targeted regions but not in another nontargeted gene, indicating that mutagenesis is targeted. A collection of these mutants has been sequenced and transitions, transversions, and frame shift mutations have been identified.